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Epicatechin
Epicatechin, containing catechins, is phytochemicals of Flavan-3-ols, in the group of Flavonoids (polyphenols), found abundantly in kola nut, tea and grapes, etc.
Health benefits
1. Testosterone
In the study of the effects of catechins on testosterone secretion in rat testicular Leydig cells (LCs) both in vivo and in vitro, found that Catechins increased plasma testosterone in vivo in male rats. In vitro, low-dose concentration of catechins increased gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release by anterior pituitary gland and hCG-stimulated testosterone release by LCs of male rats, according to "Effects of catechin, epicatechin and epigallocatechin gallate on testosterone production in rat leydig cells" by Yu PL, Pu HF, Chen SY, Wang SW, Wang PS(1)
2. Insulin Resistance
In the study of increased plasma levels of free fatty acids (FFAs) are associated with profound insulin resistance in skeletal muscle and may also play a critical role in the insulin resistance of obesity and type 2 diabetes mellitus, found that epigallocatechin gallate (EGCG) and curcumin treatment reduce insulin receptor substrate-1 (IRS-1) Ser307 phosphorylation, and curcumin is more potent to increase Akt phosphorylation in TPA induction. Moreover, we found that after 5 h of palmitate incubation, epicatechin gallate (ECG) can suppress IRS-1 Ser307 phosphorylation and significantly promote Akt, ERK1/2, p38 MAPK, and AMP-activated protein kinase activation. With a longer incubation with palmitate, IRS-1 exhibited a dramatic depletion, and treatment with EGCG, ECG, and curcumin could reverse IRS-1 expression, Akt phosphorylation, and MAPK signaling cascade activation and improve glucose uptake in C2C12 skeletal muscle cells, according to "Suppression of Free Fatty Acid-Induced Insulin Resistance by Phytopolyphenols in C2C12 Mouse Skeletal Muscle Cells" by Deng YT, Chang TW, Lee MS, Lin JK.(2)
3. Genoprotective effects
In the determination of what effects could trigger the effects of epicatechin gallate(ECG) in C6 cells, found that ECG as a dose-dependent genoprotective compound in C6 astroglial cells. This indicates that small doses of polyphenols included in our diet could have beneficial effects on neural cells, contributing to prevention of oxidative stress-associated brain pathologies. In addition, our data highlight the importance of strictly modulating doses and/or consumption of antioxidant-fortified foods or additional supplements containing such beneficial molecules, according to "Genoprotective effects of the green tea-derived polyphenol/epicatechin gallate in C6 astroglial cells' by Abib RT, Quincozes-Santos A, Zanotto C, Zeidán-Chuliá F, Lunardi PS, Gonçalves CA, Gottfried C.(3)
4. Colon cancer
In the identification of the anticarcinogenic effects of the flavanols epicatechin (EC),epicatechin-gallate (ECG) and procyanidin B2 (PB2) on Caco-2 and SW480 colon cancer cells, found that the different cytotoxicity of flavanols is caused by their different activity and the degree of differentiation of the colon cancer cell line. Thus, ECG induced apoptosis in SW480 cells and contributed to the cytotoxic effect, whereas ECG enhanced the antioxidant potential in Caco-2 cells. PB2 activated cell proliferation and survival/proliferation pathways in SW480 cells, accoridng to "Dietary flavanols exert different effects on antioxidant defenses and apoptosis/proliferation in Caco-2 and SW480 colon cancer cells" by
Ramos S, Rodríguez-Ramiro I, Martín MA, Goya L, Bravo L.(4)
5. Anti cancer
In the demonstration of the ability of monomeric and dimeric flavanols in scavenging reactive nitrogen species derived from nitrous acid, found that epicatechin was transferred across the jejunum of the small intestine yielding metabolites, its nitroso form was not absorbed. Dimer B2 but not epicatechin monomer inhibited the proliferation of, and triggered apoptosis in, Caco-2 cells. The latter was accompanied by caspase-3 activation and reductions in Akt phosphorylation, suggesting activation of apoptosis via inhibition of prosurvival signaling, according to "The reaction of flavanols with nitrous acid protects against N-nitrosamine formation and leads to the formation of nitroso derivatives which inhibit cancer cell growth" by Lee SY, Munerol B, Pollard S, Youdim KA, Pannala AS, Kuhnle GG, Debnam ES, Rice-Evans C, Spencer JP.(5)
6. Antioxidants
In the evaluation of evaluate the antioxidant response of colon-derived Caco2 cells to dietary flavanols, found that Flavanols ( epicatechin (EC), epicatechin-3-gallate (ECG), epigallocatechin-3-gallate (EGCG) and procyanidin B2 (PB2)) protect Caco2 cells against an induced oxidative stress and subsequent cellular death by reducing ROS production and preventing caspase-3 activation. In particular, PB2 increases the activity of antioxidant/detoxification enzymes and thus protects Caco2 cells by directly counteracting free radicals and also by activating the antioxidant defence system, according to "Comparative effects of dietary flavanols on antioxidant defences and their response to oxidant-induced stress on Caco2 cells" by Rodríguez-Ramiro I, Martín MA, Ramos S, Bravo L, Goya L.(6)
7. Hepatitis C virus
In the investigation of the polyphenol, epigallocatechin-3-gallate (EGCG) and and its derivatives, epigallocatechin (EGC), epicatechin gallate (ECG), and epicatechin (EC), as an inhibitor of HCV entry, found that treatment with EGCG directly during inoculation strongly inhibited HCV infectivity. Expression levels of all known HCV (co-)receptors were unaltered by EGCG. Finally, we showed that EGCG inhibits viral attachment to the cell, thus disrupting the initial step of HCV cell entry and concluded that the green tea molecule, EGCG, potently inhibits HCV entry and could be part of an antiviral strategy aimed at the prevention of HCV reinfection after liver transplantation, according to "The green tea polyphenol, epigallocatechin-3-gallate, inhibits hepatitis C virus entry" by Ciesek S, von Hahn T, Colpitts CC, Schang LM, Friesland M, Steinmann J, Manns MP, Ott M, Wedemeyer H, Meuleman P, Pietschmann T, Steinmann E.(7)
8. Genotoxic effects
In the evaluation of the potential cytotoxic and prooxidative effects of green tea extract and its two main flavonoid constituents epigallocatechin gallate (EGCG) andepicatechin gallate (ECG) on human laryngeal carcinoma cell line (HEp2), found that the cytotoxicity of EGCG and ECG increased with the time of incubation. Green tea extract induced lipid peroxidation in the CK2 cell line. The pro-oxidant effect of green tea was determined at concentrations higher than those found in traditionally prepared green tea infusions, according to "Genotoxic effects of green tea extract on human laryngeal carcinoma cells in vitro" by Durgo K, Kostić S, Gradiški K, Komes D, Osmak M, Franekić J.(8)
9. Anti inflammatory properties
In the comparison of anti-tumoral properties of EGCG on human pancreatic ductal adenocarcinoma (PDAC) cells PancTu-I, Panc1, Panc89 and BxPC3 and the effects of two minor components of green tea catechins, catechin gallate (CG) andepicatechin gallate (ECG), found that all three catechins inhibited proliferation of PDAC cells in a dose- and time-dependent manner. Interestingly, CG and ECG exerted much stronger anti-proliferative effects than EGCG. Western blot analyses performed with PancTu-I cells revealed catechin-mediated modulation of cell cycle regulatory proteins (cyclins, cyclin-dependent kinases [CDK], CDK inhibitors). Again, these effects were clearly more pronounced in CG or ECG than in EGCG-treated cells, according to "Epicatechin gallate and catechin gallate are superior to epigallocatechin gallate in growth suppression and anti-inflammatory activities in pancreatic tumor cells" by Kürbitz C, Heise D, Redmer T, Goumas F, Arlt A, Lemke J, Rimbach G, Kalthoff H, Trauzold A.(9)
10. Breast cancer
In the identification of an inverse association between the risk of breast cancer and the intake of green tea has also been reported in Asian Americans, found that Nude mice inoculated with human breast cancer MDA-MB-231 cells and treated with GTP and EGCG were effective in delaying the tumor incidence as well as reducing the tumor burden when compared to the water fed and similarly handled control. GTP and EGCG treatment were also found to induce apoptosis and inhibit the proliferation when the tumor tissue sections were examined by immunohistochemistry, according to "Green tea polyphenols and its constituent epigallocatechin gallate inhibits proliferation of human breast cancer cells in vitro and in vivo" by Thangapazham RL, Singh AK, Sharma A, Warren J, Gaddipati JP, Maheshwari RK.(10)
11. Blastocysts
In the analyzing the cytotoxic effects of epicatechin gallate (ECG), a polyphenol extract from green tea, on the blastocyst stage of mouse embryos, subsequent embryonic attachment, and in vitro and in vivo outgrowth implantation after embryo transfer, found that Blastocysts treated with 50 microM ECG exhibited a significant increase in apoptosis and a corresponding decrease in total cell number. Importantly, the implantation success rate of blastocysts pretreated with 50 microM ECG was lower than that of controls, and in vitro treatment with 50 microM ECG was associated with increased resorption of post-implantation embryos and decreased fetal weight, according to "Epicatechin gallate decreases the viability and subsequent embryonic development of mouse blastocysts" by Tu HC, Chen CP, Chan WH.(11)
12. Prostate cancer
In the examination of the HGF/c-Met pathway, an important regulator of signaling pathways responsible for invasion and metastasis of most human cancers, found that EGCG could act both by preventing activation of c-Met by HGF and by attenuating the activity of pathways already induced by HGF. HGF did not activate the MAPK and PI3-K pathways in cells treated with methyl-beta-cyclodextrin (mCD) to remove cholesterol. Furthermore, subcellular fractionation approaches demonstrated that only phosphorylated c-Met accumulated in Triton X-100 membrane insoluble fractions, supporting a role for lipid rafts in regulating c-Met signaling. Finally, EGCG treatment inhibited DiIC16 incorporation into membrane lipid ordered domains, and cholesterol partially inhibited the EGCG effects on signaling, according to "The polyphenol epigallocatechin-3-gallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cells" byDuhon D, Bigelow RL, Coleman DT, Steffan JJ, Yu C, Langston W, Kevil CG, Cardelli JA.(12)
13. Periodontal disease
in the investigation of IL-6 is well recognized to be a potent bone resorptive agent and thus in the development of periodontal disease, found that EGCG, ECG, and TFDG prevented TNFSF14-mediated IL-6 production in HGFs. EGCG, ECG, and TFDG prevented TNFSF14-induced extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor-kappaB activation in HGFs. Inhibitors of ERK, JNK, and nuclear factor-kappaB decreased TNFSF14-induced IL-6 production. In addition, EGCG, ECG, and TFDG attenuated TNFSF14 receptor expression on HGFs, according to "Tea polyphenols inhibit IL-6 production in tumor necrosis factor superfamily 14-stimulated human gingival fibroblasts" by Hosokawa Y, Hosokawa I, Ozaki K, Nakanishi T, Nakae H, Matsuo T.(13)
14. Glucose tolerance
In the investigation of the benefit of green tea extract (GTE) consumption in effecting prolonged postprandial hyperglycemia, a detrimental factor for type 2 diabetes and obesity, found that the gallated catechin when it is in the circulation elevates blood glucose level by blocking normal glucose uptake into the tissues, resulting in secondary hyperinsulinemia, whereas it decreases glucose entry into the circulation when they are inside the intestinal lumen. These findings encourage the development of non-absorbable derivatives of gallated catechins for preventative treatment of type 2 diabetes and obesity, which would specifically induce only the positive luminal effect, according to "Ambivalent role of gallated catechins in glucose tolerance in humans: a novel insight into non-absorbable gallated catechin-derived inhibitors of glucose absorption" by Park JH, Jin JY, Baek WK, Park SH, Sung HY, Kim YK, Lee J, Song DK.(13)
14. Etc.
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/20432242
(2) http://www.ncbi.nlm.nih.gov/pubmed/22191431
(3) http://www.ncbi.nlm.nih.gov/pubmed/20828315
(4) http://www.ncbi.nlm.nih.gov/pubmed/21945981
(5) http://www.ncbi.nlm.nih.gov/pubmed/16413414
(6) http://www.ncbi.nlm.nih.gov/pubmed/21046126
(7) http://www.ncbi.nlm.nih.gov/pubmed/21837753
(8) http://www.ncbi.nlm.nih.gov/pubmed/21705301
(9) http://www.ncbi.nlm.nih.gov/pubmed/21241417
(10) http://www.ncbi.nlm.nih.gov/pubmed/16519995
(11) http://www.ncbi.nlm.nih.gov/pubmed/20708524
(12) http://www.ncbi.nlm.nih.gov/pubmed/20623641
(13) http://www.ncbi.nlm.nih.gov/pubmed/20461739
(14) http://www.ncbi.nlm.nih.gov/pubmed/20065503
